camel milk triggers apoptotic signaling pathways in human hepatoma hepg2 and breast cancer mcf7 cell lines through transcriptional mechanism骆驼奶触发凋亡信号通路在人类肝癌hepg2和乳腺癌mcf7细胞通过转录机制.pdfVIP
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camel milk triggers apoptotic signaling pathways in human hepatoma hepg2 and breast cancer mcf7 cell lines through transcriptional mechanism骆驼奶触发凋亡信号通路在人类肝癌hepg2和乳腺癌mcf7细胞通过转录机制
Hindawi Publishing Corporation
Journal of Biomedicine and Biotechnology
Volume 2012, Article ID 593195, 9 pages
doi:10.1155/2012/593195
Research Article
Camel Milk Triggers Apoptotic Signaling Pathways in
Human Hepatoma HepG2 and Breast Cancer MCF7 Cell Lines
through Transcriptional Mechanism
Hesham M. Korashy,1 Zaid H. Maayah,1 Adel R. Abd-Allah,1
Ayman O. S. El-Kadi,2 and Abdulqader A. Alhaider3
1 Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia
2 Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, AB, Canada T6G 2E1
3 Department of Pharmacology, College of Medicine, King Saud University, Riyadh 11461, Saudi Arabia
Correspondence should be addressed to Abdulqader A. Alhaider, aqahaider@
Received 24 November 2011; Accepted 27 January 2012
Academic Editor: Kazim Husain
Copyright © 2012 Hesham M. Korashy et al. This is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.
Few published studies have reported the use of crude camel milk in the treatment of stomach infections, tuberculosis and cancer.
Yet, little research was conducted on the effect of camel milk on the apoptosis and oxidative stress associated with human cancer.
The present study investigated the effect and the underlying mechanisms of camel milk on the proliferation of human cancer cells
using an in vitro model of human hepatoma (HepG2) and human breast (MCF7) cancer cells. Our results showed that camel
milk, but not bovine milk, significantly inhibited HepG2 and MCF7 cells proliferation through the activation of caspase-3 mRNA
and activity levels, and
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